The heat-shock response in vivo: experimental induction during mammalian organogenesis.
The heat-shock response in vivo: experimental induction during mammalian organogenesis.
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体内热休克反应：哺乳动物器官发生过程中的实验诱导。
DOI：
10.1002/tcm.1770060609
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Banerjee,D
中科院分区：
文献类型：
--
作者：
German,J;Louie,E;Banerjee,D
根据畸胎症的胚胎应激假说，解剖畸形可能是胚胎在器官决定或分化的某个关键阶段诱导热休克反应（HSR）的结果。这一假说认为，致畸原是(1)能够诱导HSR和(2)能够到达发育中的胚胎的任何物质。作为确定该假设是否成立的第一步，有必要确定胚胎在器官发生期间是否实际上能够产生HSR。怀孕的老鼠用两种经典的HSR诱导剂治疗，一种是物理诱导剂，另一种是化学诱导剂，即热疗和亚砷酸钠。当这些胚胎还在活体小鼠体内时，它们对热休克蛋白诱导有反应，对照骨髓也是如此。
According to the embryonic stress hypothesis of teratogenesis, anatomical malformation can be the consequence of the induction of a heat‐shock response (HSR) in the embryo at some critical stage during the determination or differentiation of organs. This hypothesis states that a teratogen is any agent (i) that is capable of inducing a HSR and (ii) that can reach the developing embryo. As a first step in determining whether the hypothesis is tenable, it was necessary to determine whether the embryo in fact is capable of making the HSR during the period of organogenesis. Pregnant mice were treated with two classical inducers of the HSR, one a physical and the other a chemical agent—namely, hyperthermia and sodium arsenite. The embryos, while still in the living mouse, responded with heat‐shock protein induction, as did control bone marrow.